ReviewDrugs2016
Targeting Select Cellular Stress Pathways to Prevent Hyperglycemia-Related Complications: Shifting the Paradigm.
Review in Drugs, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Cardiomodulatory Effects of Cardiometabolic and Antihyperglycemic Medications: The Roles of Oxidative and Endoplasmic Reticulum Stress.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2025Review
- Reduced cellular glucose transport confers natural protection against dextrose-induced superoxide generation and endoplasmic reticulum stress in domestic hen.Physiological reports · 2021Article
- Demystifying Oxidative Stress.Handbook of experimental pharmacology · 2021Article
- Diabetes, Hypertension, and Cardiovascular Disease: Clinical Insights and Vascular Mechanisms.The Canadian journal of cardiology · 2018Review
- Eucalyptol ameliorates Snail1/β-catenin-dependent diabetic disjunction of renal tubular epithelial cells and tubulointerstitial fibrosis.Oncotarget · 2017Article
- Stabilization of endogenous Nrf2 by minocycline protects against Nlrp3-inflammasome induced diabetic nephropathy.Scientific reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the advances made in preventing complications of diabetes, there is still substantial residual risk. Hence the need for developing new therapeutic agents that target the various facets of the pathogenesis of complications in people with diabetes. Traditionally four general biochemical pathways had been recognized as major contributors to glucotoxicity. These include the polyol pathway, the protein kinase C (PKC) pathway, glycosylation pathway, and oxidative stress. The latter has been proposed as a common impetus of the other pathways of glucotoxicity. More recently, the cross talk between oxidative stress and other recognized cellular stresses such as endoplasmic reticulum (ER), inflammatory, and mitochondrial stresses has emerged as an important additional mechanism of glucotoxicity. The observation that targeting oxidative stress with antioxidants has been associated with unfavorable clinical outcomes and the recognition that in cell cultures antioxidants may aggravate ER stress, suggests that selective targeting of individual cellular stresses may not be sufficient for preventing glucotoxicity. Future efforts should focus on developing therapeutic agents that can ameliorate cellular stress globally by simultaneously targeting the oxidative, ER, mitochondrial, and inflammatory stresses.
Indexed as
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What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.